Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice

Autores: Wolf, Dennis; Hohmann, Jan David; Wiedemann, Ansgar; Bledzka, Kamila; Blankenbach, Hermann; Marchini, Timoteo Oscar; Gutte, Katharina; Zeschky, Katharina; Bassler, Nicole; Hoppe, Natalie; Rodriguez, Alexandra Ortiz; Herr, Nadine; Hilgendorf, Ingo; Stachon, Peter; Willecke, Florian; Duerschmied, Daniel; von zur Muhlen, Constantin; Soloviev, Dmitry A.; Zhang, Li; Bode, Christoph; Plow, Edward F.; Libby, Peter; Peter, Karlheinz; Zirlik, Andreas
Año de publicación: 2011
Idioma: inglés
Tipo de recurso: artículo
Estado: versión publicada
Descripción: Rationale: CD40L figures prominently in chronic inflammatory diseases such as atherosclerosis. However, since CD40L potently regulates immune function and hemostasis by interaction with CD40 receptor and the platelet integrin GPIIb/IIIa, its global inhibition compromises host defense and generated thromboembolic complications in clinical trials. We recently reported that CD40L mediates atherogenesis independently of CD40 and proposed Mac-1 as an alternate receptor. Objective: Here, we molecularly characterized the CD40L-Mac-1 interaction and tested whether its selective inhibition by a small peptide modulates inflammation and atherogenesis in vivo. Methods and Results: CD40L concentration-dependently bound to Mac-1 I-domain in solid phase binding assays, and a high-affinity interaction was revealed by surface-plasmon-resonance analysis. We identified the motif EQLKKSKTL, an exposed loop between the α1 helix and the β-sheet B, on Mac-1 as binding site for CD40L. A linear peptide mimicking this sequence, M7, specifically inhibited the interaction of CD40L and Mac-1. A cyclisized version optimized for in vivo use, cM7, decreased peritoneal inflammation and inflammatory cell recruitment in vivo. Finally, LDLr -/- mice treated with intraperitoneal injections of cM7 developed smaller, less inflamed atherosclerotic lesions featuring characteristics of stability. However, cM7 did not interfere with CD40L-CD40 binding in vitro and CD40L-GPIIb/IIIa-mediated thrombus formation in vivo. Conclusions: We present the novel finding that CD40L binds to the EQLKKSKTL motif on Mac-1 mediating leukocyte recruitment and atherogenesis. Specific inhibition of CD40L-Mac-1 binding may represent an attractive anti-inflammatory treatment strategy for atherosclerosis and other inflammatory conditions, potentially avoiding the unwanted immunologic and thrombotic effects of global inhibition of CD40L.
Fil: Wolf, Dennis. Albert-Ludwigs-Universität Freiburg; Alemania. Baker IDI Heart and Diabetes Institute; Australia
Fil: Hohmann, Jan David. Baker IDI Heart and Diabetes Institute; Australia
Fil: Wiedemann, Ansgar. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Bledzka, Kamila. Cleveland Clinic. Department of Molecular Cardiology; Estados Unidos
Fil: Blankenbach, Hermann. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Marchini, Timoteo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Gutte, Katharina. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Zeschky, Katharina. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Bassler, Nicole. Baker IDI Heart and Diabetes Institute; Australia
Fil: Hoppe, Natalie. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Rodriguez, Alexandra Ortiz. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Herr, Nadine. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Hilgendorf, Ingo. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Stachon, Peter. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Willecke, Florian. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Duerschmied, Daniel. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: von zur Muhlen, Constantin. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Soloviev, Dmitry A.. Cleveland Clinic. Department of Molecular Cardiology; Estados Unidos
Fil: Zhang, Li. University of Maryland; Estados Unidos
Fil: Bode, Christoph. Albert-Ludwigs-Universität Freiburg; Alemania
Fil: Plow, Edward F.. Cleveland Clinic. Department of Molecular Cardiology; Estados Unidos
Fil: Libby, Peter. Harvard Medical School; Estados Unidos
Fil: Peter, Karlheinz. Baker IDI Heart and Diabetes Institute; Australia
Fil: Zirlik, Andreas. Albert-Ludwigs-Universität Freiburg; Alemania
Materia: Atherosclerosis
Cd40l
Inflammation
Mac-1
Peptide Inhibitor
Nivel de accesibilidad: acceso abierto
Condiciones de uso: https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
Institución: Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador: oai:ri.conicet.gov.ar:11336/67807

Acceder

id	CONICETDig_f5b9de1fb719598fd2031b55f9230f81
oai_identifier_str	oai:ri.conicet.gov.ar:11336/67807
network_acronym_str	CONICETDig
repository_id_str	3498
network_name_str	CONICET Digital (CONICET)
spelling	Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in miceWolf, DennisHohmann, Jan DavidWiedemann, AnsgarBledzka, KamilaBlankenbach, HermannMarchini, Timoteo OscarGutte, KatharinaZeschky, KatharinaBassler, NicoleHoppe, NatalieRodriguez, Alexandra OrtizHerr, NadineHilgendorf, IngoStachon, PeterWillecke, FlorianDuerschmied, Danielvon zur Muhlen, ConstantinSoloviev, Dmitry A.Zhang, LiBode, ChristophPlow, Edward F.Libby, PeterPeter, KarlheinzZirlik, AndreasAtherosclerosisCd40lInflammationMac-1Peptide Inhibitorhttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Rationale: CD40L figures prominently in chronic inflammatory diseases such as atherosclerosis. However, since CD40L potently regulates immune function and hemostasis by interaction with CD40 receptor and the platelet integrin GPIIb/IIIa, its global inhibition compromises host defense and generated thromboembolic complications in clinical trials. We recently reported that CD40L mediates atherogenesis independently of CD40 and proposed Mac-1 as an alternate receptor. Objective: Here, we molecularly characterized the CD40L-Mac-1 interaction and tested whether its selective inhibition by a small peptide modulates inflammation and atherogenesis in vivo. Methods and Results: CD40L concentration-dependently bound to Mac-1 I-domain in solid phase binding assays, and a high-affinity interaction was revealed by surface-plasmon-resonance analysis. We identified the motif EQLKKSKTL, an exposed loop between the α1 helix and the β-sheet B, on Mac-1 as binding site for CD40L. A linear peptide mimicking this sequence, M7, specifically inhibited the interaction of CD40L and Mac-1. A cyclisized version optimized for in vivo use, cM7, decreased peritoneal inflammation and inflammatory cell recruitment in vivo. Finally, LDLr -/- mice treated with intraperitoneal injections of cM7 developed smaller, less inflamed atherosclerotic lesions featuring characteristics of stability. However, cM7 did not interfere with CD40L-CD40 binding in vitro and CD40L-GPIIb/IIIa-mediated thrombus formation in vivo. Conclusions: We present the novel finding that CD40L binds to the EQLKKSKTL motif on Mac-1 mediating leukocyte recruitment and atherogenesis. Specific inhibition of CD40L-Mac-1 binding may represent an attractive anti-inflammatory treatment strategy for atherosclerosis and other inflammatory conditions, potentially avoiding the unwanted immunologic and thrombotic effects of global inhibition of CD40L.Fil: Wolf, Dennis. Albert-Ludwigs-Universität Freiburg; Alemania. Baker IDI Heart and Diabetes Institute; AustraliaFil: Hohmann, Jan David. Baker IDI Heart and Diabetes Institute; AustraliaFil: Wiedemann, Ansgar. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Bledzka, Kamila. Cleveland Clinic. Department of Molecular Cardiology; Estados UnidosFil: Blankenbach, Hermann. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Marchini, Timoteo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Gutte, Katharina. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Zeschky, Katharina. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Bassler, Nicole. Baker IDI Heart and Diabetes Institute; AustraliaFil: Hoppe, Natalie. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Rodriguez, Alexandra Ortiz. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Herr, Nadine. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Hilgendorf, Ingo. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Stachon, Peter. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Willecke, Florian. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Duerschmied, Daniel. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: von zur Muhlen, Constantin. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Soloviev, Dmitry A.. Cleveland Clinic. Department of Molecular Cardiology; Estados UnidosFil: Zhang, Li. University of Maryland; Estados UnidosFil: Bode, Christoph. Albert-Ludwigs-Universität Freiburg; AlemaniaFil: Plow, Edward F.. Cleveland Clinic. Department of Molecular Cardiology; Estados UnidosFil: Libby, Peter. Harvard Medical School; Estados UnidosFil: Peter, Karlheinz. Baker IDI Heart and Diabetes Institute; AustraliaFil: Zirlik, Andreas. Albert-Ludwigs-Universität Freiburg; AlemaniaAmerican Heart Association2011-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/67807Wolf, Dennis; Hohmann, Jan David; Wiedemann, Ansgar; Bledzka, Kamila; Blankenbach, Hermann; et al.; Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice; American Heart Association; Circulation Research; 109; 11; 11-2011; 1269-12790009-7330CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1161/CIRCRESAHA.111.247684info:eu-repo/semantics/altIdentifier/url/https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.111.247684info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:00:20Zoai:ri.conicet.gov.ar:11336/67807instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:00:20.284CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv	Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice
title	Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice
spellingShingle	Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice Wolf, Dennis Atherosclerosis Cd40l Inflammation Mac-1 Peptide Inhibitor
title_short	Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice
title_full	Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice
title_fullStr	Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice
title_full_unstemmed	Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice
title_sort	Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice
dc.creator.none.fl_str_mv	Wolf, Dennis Hohmann, Jan David Wiedemann, Ansgar Bledzka, Kamila Blankenbach, Hermann Marchini, Timoteo Oscar Gutte, Katharina Zeschky, Katharina Bassler, Nicole Hoppe, Natalie Rodriguez, Alexandra Ortiz Herr, Nadine Hilgendorf, Ingo Stachon, Peter Willecke, Florian Duerschmied, Daniel von zur Muhlen, Constantin Soloviev, Dmitry A. Zhang, Li Bode, Christoph Plow, Edward F. Libby, Peter Peter, Karlheinz Zirlik, Andreas
author	Wolf, Dennis
author_facet	Wolf, Dennis Hohmann, Jan David Wiedemann, Ansgar Bledzka, Kamila Blankenbach, Hermann Marchini, Timoteo Oscar Gutte, Katharina Zeschky, Katharina Bassler, Nicole Hoppe, Natalie Rodriguez, Alexandra Ortiz Herr, Nadine Hilgendorf, Ingo Stachon, Peter Willecke, Florian Duerschmied, Daniel von zur Muhlen, Constantin Soloviev, Dmitry A. Zhang, Li Bode, Christoph Plow, Edward F. Libby, Peter Peter, Karlheinz Zirlik, Andreas
author_role	author
author2	Hohmann, Jan David Wiedemann, Ansgar Bledzka, Kamila Blankenbach, Hermann Marchini, Timoteo Oscar Gutte, Katharina Zeschky, Katharina Bassler, Nicole Hoppe, Natalie Rodriguez, Alexandra Ortiz Herr, Nadine Hilgendorf, Ingo Stachon, Peter Willecke, Florian Duerschmied, Daniel von zur Muhlen, Constantin Soloviev, Dmitry A. Zhang, Li Bode, Christoph Plow, Edward F. Libby, Peter Peter, Karlheinz Zirlik, Andreas
author2_role	author author author author author author author author author author author author author author author author author author author author author author author
dc.subject.none.fl_str_mv	Atherosclerosis Cd40l Inflammation Mac-1 Peptide Inhibitor
topic	Atherosclerosis Cd40l Inflammation Mac-1 Peptide Inhibitor
purl_subject.fl_str_mv	https://purl.org/becyt/ford/3.2 https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv	Rationale: CD40L figures prominently in chronic inflammatory diseases such as atherosclerosis. However, since CD40L potently regulates immune function and hemostasis by interaction with CD40 receptor and the platelet integrin GPIIb/IIIa, its global inhibition compromises host defense and generated thromboembolic complications in clinical trials. We recently reported that CD40L mediates atherogenesis independently of CD40 and proposed Mac-1 as an alternate receptor. Objective: Here, we molecularly characterized the CD40L-Mac-1 interaction and tested whether its selective inhibition by a small peptide modulates inflammation and atherogenesis in vivo. Methods and Results: CD40L concentration-dependently bound to Mac-1 I-domain in solid phase binding assays, and a high-affinity interaction was revealed by surface-plasmon-resonance analysis. We identified the motif EQLKKSKTL, an exposed loop between the α1 helix and the β-sheet B, on Mac-1 as binding site for CD40L. A linear peptide mimicking this sequence, M7, specifically inhibited the interaction of CD40L and Mac-1. A cyclisized version optimized for in vivo use, cM7, decreased peritoneal inflammation and inflammatory cell recruitment in vivo. Finally, LDLr -/- mice treated with intraperitoneal injections of cM7 developed smaller, less inflamed atherosclerotic lesions featuring characteristics of stability. However, cM7 did not interfere with CD40L-CD40 binding in vitro and CD40L-GPIIb/IIIa-mediated thrombus formation in vivo. Conclusions: We present the novel finding that CD40L binds to the EQLKKSKTL motif on Mac-1 mediating leukocyte recruitment and atherogenesis. Specific inhibition of CD40L-Mac-1 binding may represent an attractive anti-inflammatory treatment strategy for atherosclerosis and other inflammatory conditions, potentially avoiding the unwanted immunologic and thrombotic effects of global inhibition of CD40L. Fil: Wolf, Dennis. Albert-Ludwigs-Universität Freiburg; Alemania. Baker IDI Heart and Diabetes Institute; Australia Fil: Hohmann, Jan David. Baker IDI Heart and Diabetes Institute; Australia Fil: Wiedemann, Ansgar. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Bledzka, Kamila. Cleveland Clinic. Department of Molecular Cardiology; Estados Unidos Fil: Blankenbach, Hermann. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Marchini, Timoteo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Gutte, Katharina. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Zeschky, Katharina. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Bassler, Nicole. Baker IDI Heart and Diabetes Institute; Australia Fil: Hoppe, Natalie. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Rodriguez, Alexandra Ortiz. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Herr, Nadine. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Hilgendorf, Ingo. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Stachon, Peter. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Willecke, Florian. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Duerschmied, Daniel. Albert-Ludwigs-Universität Freiburg; Alemania Fil: von zur Muhlen, Constantin. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Soloviev, Dmitry A.. Cleveland Clinic. Department of Molecular Cardiology; Estados Unidos Fil: Zhang, Li. University of Maryland; Estados Unidos Fil: Bode, Christoph. Albert-Ludwigs-Universität Freiburg; Alemania Fil: Plow, Edward F.. Cleveland Clinic. Department of Molecular Cardiology; Estados Unidos Fil: Libby, Peter. Harvard Medical School; Estados Unidos Fil: Peter, Karlheinz. Baker IDI Heart and Diabetes Institute; Australia Fil: Zirlik, Andreas. Albert-Ludwigs-Universität Freiburg; Alemania
description	Rationale: CD40L figures prominently in chronic inflammatory diseases such as atherosclerosis. However, since CD40L potently regulates immune function and hemostasis by interaction with CD40 receptor and the platelet integrin GPIIb/IIIa, its global inhibition compromises host defense and generated thromboembolic complications in clinical trials. We recently reported that CD40L mediates atherogenesis independently of CD40 and proposed Mac-1 as an alternate receptor. Objective: Here, we molecularly characterized the CD40L-Mac-1 interaction and tested whether its selective inhibition by a small peptide modulates inflammation and atherogenesis in vivo. Methods and Results: CD40L concentration-dependently bound to Mac-1 I-domain in solid phase binding assays, and a high-affinity interaction was revealed by surface-plasmon-resonance analysis. We identified the motif EQLKKSKTL, an exposed loop between the α1 helix and the β-sheet B, on Mac-1 as binding site for CD40L. A linear peptide mimicking this sequence, M7, specifically inhibited the interaction of CD40L and Mac-1. A cyclisized version optimized for in vivo use, cM7, decreased peritoneal inflammation and inflammatory cell recruitment in vivo. Finally, LDLr -/- mice treated with intraperitoneal injections of cM7 developed smaller, less inflamed atherosclerotic lesions featuring characteristics of stability. However, cM7 did not interfere with CD40L-CD40 binding in vitro and CD40L-GPIIb/IIIa-mediated thrombus formation in vivo. Conclusions: We present the novel finding that CD40L binds to the EQLKKSKTL motif on Mac-1 mediating leukocyte recruitment and atherogenesis. Specific inhibition of CD40L-Mac-1 binding may represent an attractive anti-inflammatory treatment strategy for atherosclerosis and other inflammatory conditions, potentially avoiding the unwanted immunologic and thrombotic effects of global inhibition of CD40L.
publishDate	2011
dc.date.none.fl_str_mv	2011-11
dc.type.none.fl_str_mv	info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo
format	article
status_str	publishedVersion
dc.identifier.none.fl_str_mv	http://hdl.handle.net/11336/67807 Wolf, Dennis; Hohmann, Jan David; Wiedemann, Ansgar; Bledzka, Kamila; Blankenbach, Hermann; et al.; Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice; American Heart Association; Circulation Research; 109; 11; 11-2011; 1269-1279 0009-7330 CONICET Digital CONICET
url	http://hdl.handle.net/11336/67807
identifier_str_mv	Wolf, Dennis; Hohmann, Jan David; Wiedemann, Ansgar; Bledzka, Kamila; Blankenbach, Hermann; et al.; Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice; American Heart Association; Circulation Research; 109; 11; 11-2011; 1269-1279 0009-7330 CONICET Digital CONICET
dc.language.none.fl_str_mv	eng
language	eng
dc.relation.none.fl_str_mv	info:eu-repo/semantics/altIdentifier/doi/10.1161/CIRCRESAHA.111.247684 info:eu-repo/semantics/altIdentifier/url/https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.111.247684
dc.rights.none.fl_str_mv	info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv	openAccess
rights_invalid_str_mv	https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv	application/pdf application/pdf application/pdf
dc.publisher.none.fl_str_mv	American Heart Association
publisher.none.fl_str_mv	American Heart Association
dc.source.none.fl_str_mv	reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str	CONICET Digital (CONICET)
collection	CONICET Digital (CONICET)
instname_str	Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv	CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv	dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_	1844613783024041984
score	13.070432

Binding of CD40L to Mac-1's i-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis-but does not affect immunity and thrombosis in mice

Publicaciones similares